作者机构：
[Jiao, Liqun; Xu, Ran; Yang, Bin; Wang, Tao; Luo, Jichang; Ma, Yan] China Int Neurosci Inst China INI, Beijing, Peoples R China.;[Jiao, Liqun; Xu, Ran; Yang, Bin; Wang, Tao; Luo, Jichang; Ma, Yan] Capital Med Univ, Dept Neurosurg, Xuanwu Hosp, Beijing, Peoples R China.;[Liao, Wanying] Chinese Acad Med Sci & Peking Union Med Coll, Peking Union Med Coll Hosp, Beijing, Peoples R China.;[Wang, Xue] Capital Med Univ, Xuanwu Hosp, Med Lib, Beijing, Peoples R China.;[Li, Wei] Liaocheng Peoples Hosp, Dept Neurosurg, Liaocheng, Shandong, Peoples R China.
通讯机构：
[Yang, B.; Jiao, L.] C;China International Neuroscience Institute (China-INI)China
关键词：
CLINICAL PHARMACOLOGY;Coronary heart disease;Lipid disorders;Protocols & guidelines;VASCULAR MEDICINE
期刊：
Archives of Toxicology,2022年96(12):3245-3255 ISSN：0340-5761
通讯作者：
Wen-Liang Liu<&wdkj&>Jian-Ye Yan<&wdkj&>Xiong Cai
作者机构：
[Cai, Xiong; Wu, Han; Yi, Ou-Yang; Yan, Jian-Ye; Deng, Guiming; Zhang, Er-Bing; Huang, Hong] Hunan Univ Chinese Med, Hosp 1, Dept Rheumatol, Changsha 410007, Hunan, Peoples R China.;[Cai, Xiong; Wu, Han; Yi, Ou-Yang; Yan, Jian-Ye; Deng, Guiming; Zhang, Er-Bing; Huang, Hong] Hunan Univ Chinese Med, Inst Innovat & Appl Res Chinese Med, Changsha 410007, Hunan, Peoples R China.;[Liu, Wen-Liang; Zhang, Er-Bing] Shenzhen Inst Drug Control, Shenzhen 518057, Guangdong, Peoples R China.;[Huang, Yu-Ming] Hunan Zhengqing Pharmaceut Grp Co Ltd, Huaihua 418000, Hunan, Peoples R China.
通讯机构：
[Wen-Liang Liu] S;[Jian-Ye Yan; Xiong Cai] D;Shenzhen Institute for Drug Control, Shenzhen, China<&wdkj&>Department of Rheumatology of the First Hospital and Institute of Innovation and Applied Research in Chinese Medicine, Hunan University of Chinese Medicine, Changsha, China<&wdkj&>Department of Rheumatology of the First Hospital and Institute of Innovation and Applied Research in Chinese Medicine, Hunan University of Chinese Medicine, Changsha, China
摘要：
Sinomenine is a bioactive alkaloid isolated from the Chinese medicinal plant Sinomenium acutum (Thunb.) Rehd. et Wils which exhibits significant analgesic, anti-inflammatory, and immunosuppressive effects. Sinomenine hydrochloride (SH) preparations, classified as natural disease-modifying antirheumatic drugs, are currently available for the treatment of rheumatoid arthritis and other rheumatic diseases. Our toxicity evaluation demonstrated that the median lethal dose of SH in female Sprague-Dawley (SD) rats was over 11 times greater than that in male SD rats, revealing striking sex-linked differences in the safety profile of SH. The present study was designed to investigate differences in the pharmacokinetics (PKs) and tissue distribution of SH between male and female SD rats after a single oral dose of 25mg/kg. PK and tissue distribution studies were performed using a validated UPLC-MS/MS method. The results showed that SH-treated SD female rats displayed markedly greater drug exposure, and SH exhibited a longer half-life and slower clearance rate than comparable studies in male rats. Moreover, the tissue distribution study confirmed that the sinomenine concentration in female rats was considerably greater in the internal organs than in male rats. Our study demonstrates, for the first time, significant sex-related differences in the safety profile and PKs of SH, which may be associated with a distinct sex-dependent metabolic mechanism of sinomenine.
期刊：
European Journal of Pharmacology,2022年930:175149 ISSN：0014-2999
通讯作者：
Sheng Xie<&wdkj&>Yu-Hong Wang
作者机构：
[Li, Zi-Rong] Guangxi Univ Chinese Med, Affiliated Hosp 1, Dept Neurol, Nanning 530022, Guangxi, Peoples R China.;[Liu, De-Guo] Guangxi Univ Chinese Med, Affiliated Hosp 1, Dept Breast Surg, Nanning 530022, Guangxi, Peoples R China.;[Xie, Sheng] Guangxi Univ Chinese Med, Affiliated Hosp 1, Prevent Dis Tradit Chinese Med Ctr, Nanning 530022, Guangxi, Peoples R China.;[Li, Chun-Yan; Wang, Yu-Hong; Zou, Man-Shu] Hunan Univ Chinese Med, State Key Lab Chinese Med Powder & Med Innovat Hun, Changsha 410208, Hunan, Peoples R China.;[Han, Yuan-Shan] Hunan Univ Chinese Med, Affiliated Hosp 1, Dept Expt, Ctr Med Innovat, Changsha 410021, Hunan, Peoples R China.
通讯机构：
[Sheng Xie] P;[Yu-Hong Wang] S;Prevention of Diseases with Traditional Chinese Medicine Center, The First Affiliated Hospital of Guangxi University of Chinese Medicine, Guangxi, Nanning, 530022, China<&wdkj&>State Key Laboratory of Chinese Medicine Powder and Medicine Innovation in Hunan (incubation), Hunan University of Chinese Medicine, Hunan, Changsha, 410208, China
摘要：
There has been ample research showing that insomnia is a potential trigger of depression as well as a symptom of depression. These two factors contribute to behavioural problems and are closely related to the plasticity of hippocampal synapses. Although depression and insomnia impair hippocampal synaptic plasticity, the mechanism by which this happens remains a mystery. This study aimed to investigate the pathogenesis of insomnia comorbidity in depression and the regulatory effect of venlafaxine combined with melatonin on hippocampal synaptic plasticity in chronic unpredictable mild stress (CUMS) with sleep deprivation (SD) rats. Thus, rats were subjected to 14 days of chronic mild unpredictable stress, gradually acclimated to sleep deprivation on days 12-14. Followed by 21 consecutive days of sleep deprivation, 18h per day, with daily gavage of venlafaxine (13.5mg/kg)+melatonin (72mg/kg) on days 15-36. Venlafaxine+melatonin treatment improves depression-like behaviour, pentobarbital sodium experimental sleep latency, and sleep duration in CUMS+SD rats. In addition to improving depressive-like behaviors, sleep deprivation also upregulates the expression of caspase-specific cysteine protein 3 (Caspase 3) in the pineal glial cells of chronic mild rats, as well as in hippocampal microglia. Expression of ionic calcium-binding adaptor 1 (iba-1), downregulates the secretion of several synaptic plasticity-related proteins, notably cAMP response element binding protein (CREB), glial cell line-derived neurotrophic factor (GDNF), and the synaptic scaffolding protein Spinophiline (Spinophiline). Hematoxylin-eosin staining showed that the structure of the pineal gland and hippocampus was damaged, and Golgi staining showed that the dendrites and spines in the DG area of the hippocampus were destroyed, vaguely aggregated or even disappeared, and the connection network could not be established. Western blot analysis further revealed a positive correlation between low melatonin levels and reduced Spinophiline protein. Interestingly, venlafaxine+melatonin reversed these events by promoting hippocampal synaptic plasticity by regulating melatonin secretion from the pineal gland. Therefore, it exerted an antidepressant effect in sleep deprivation combined with CUMS model rats. Overall, the results of this study suggest that the pathophysiology of depressive insomnia comorbidity is mediated by impaired pineal melatonin secretion and impaired hippocampal synaptic plasticity. In addition, these responses are associated with melatonin secretion from the pineal gland.
期刊：
Computational and Mathematical Methods in Medicine,2022年2022:3459102 ISSN：1748-6718
通讯作者：
Le Ma
作者机构：
[Ma, Le] Hunan Univ Chinese Med, Hosp 1, Dept Dermatol, Changsha 410007, Hunan, Peoples R China.
关键词：
Introduction;Materials and Methods;Results;Discussion;Conclusion;Abstract;Data Availability;Additional Points;Ethical Approval;Consent;Disclosure;Conflicts of Interests;Authors’ Contributions;Funding Statement;Acknowledgements;Acknowledgments;Supplementary Materials;Reference;Dataset Description;Dataset Files;Abstract;Introduction;Introduction and Materials;Introduction and Methods;Materials;Materials and Methods;Methods;Results;Discussion;Results and Discussion;Discussion and Conclusion;Results and Conclusion;Conclusion;Conclusions;Data Availability;Additional Points;Ethical Approval;Consent;Disclosure;Conflicts of Interest;Authors’ Contributions;Funding Statement;Acknowledgements;Supplementary Materials;References;Appendix;Abbreviations;Preliminaries;Introduction and Preliminaries;Notation;Proof of Theorem;Proofs;Analysis of Results;Examples;Numerical Example;Applications;Numerical Simulation;Model;Model Formulation;Systematic Palaeontology;Nomenclatural Acts;Taxonomic Implications;Experimental;Synthesis;Overview;Characterization;Background;Experimental;Theories;Calculations;Model Verification;Model Implementation;Geographic location;Study Area;Geological setting;Data Collection;Field Testing;Data and Sampling;Dataset;Literature Review;Related Works;Related Work;System Model;Methods and Data;Experimental Results;Results and Analysis;Evaluation;Implementation;Case Presentation;Case Report;Search Terms;Case Description;Case Series;Background;Limitations;Additional Points;Case;Case 1;Case 2 etc.;Concern Details;Retraction Details;Copyright;Related Articles
摘要：
Objective. Presently, astragalus polysaccharide (APS) is being investigated for its therapeutic potential in various diseases; however, its underlying mechanism has not yet been clarified. This study was aimed at observing the effects of APS on wound healing in diabetic rats and at exploring its underlying mechanism. Methods. Streptozotocin was injected into the tail vein of SD rats to induce diabetic animal models, in which an incision on the back was made. Rats were treated with different dosages of APS to observe their wound healing. Additionally, RT-qPCR and Western blot assay were conducted to observe the expression levels of PTEN and mTOR pathway-associated factors. Results. Diabetic rats had a prolonged wound healing process, fewer blood vessels, and increased inflammatory response, in which decreased PTEN and elevated mTOR phosphorylation were also identified. APS effectively improved wound healing in a dose-dependent manner by inhibiting the release of inflammatory mediators and attenuating endothelial injuries. Suppression of PTEN could effectively increase the phosphorylation of mTOR and diminish the therapeutic functions of APS on wound healing in diabetic rats. Conclusion. This study highlighted that APS could promote wound healing in diabetic rats by upregulating PTEN and suppressing the mTOR pathway activation.
作者机构：
[Li, Hongfang; Gong, Yongzhen; Shi, Yaning; Liao, Duanfang; Gu, Jia; Zhang, Chanjuan; Qin, Li] Hunan Univ Chinese Med, Sch Pharm, Lab Stem Cell Regulat Chinese Med & Its Applicat, Changsha 410208, Hunan, Peoples R China.;[Wang, Wei; Zhang, Chanjuan] Hunan Univ Chinese Med, Innovat Mat Med Res Inst, TCM & Ethnomed Innovat & Dev Int Lab, Changsha 410208, Hunan, Peoples R China.;[Zhu, Neng] Hunan Univ Chinese Med, Hosp 1, Changsha 410021, Hunan, Peoples R China.;[Dai, Aiguo; Qin, Li] Hunan Univ Chinese Med, Inst Key Lab Vasc Biol & Translat Med Hunan Prov, Changsha 410208, Hunan, Peoples R China.;[Qin, Li] Hunan Univ Chinese Med, Hunan Prov Engn Res Ctr Bioact Subst Discovery Tr, Changsha 410208, Hunan, Peoples R China.
通讯机构：
[Wei Wang] T;[Aiguo Dai] I;[Li Qin] L;TCM and Ethnomedicine Innovation & Development International Laboratory, Innovative Materia Medica Research Institute, Hunan University of Chinese Medicine, Changsha, Hunan, 410208, PR China<&wdkj&>Institutional Key Laboratory of Vascular Biology and Translational Medicine in Hunan Province, Hunan University of Chinese Medicine, Changsha, Hunan, 410208, PR China<&wdkj&>Laboratory of Stem Cell Regulation with Chinese Medicine and Its Application, School of Pharmacy, Hunan University of Chinese Medicine, Changsha, Hunan, 410208, PR China<&wdkj&>Institutional Key Laboratory of Vascular Biology and Translational Medicine in Hunan Province, Hunan University of Chinese Medicine, Changsha, Hunan, 410208, PR China<&wdkj&>Hunan Province Engineering Research Center of Bioactive Substance Discovery of Traditional Chinese Medicine, Hunan University of Chinese Medicine, Changsha, Hunan, 410208, PR China
作者机构：
[Liu, Yu] Cent South Univ, Xiangya Hosp 3, Postdoctoral Res Stn Clin Med, Changsha 410000, Hunan, Peoples R China.;[Liu, Yu; Zhou, Jian-Da; Wang, Chu-Wang] Cent South Univ, Xiangya Hosp 3, Dept Plast Surg, Changsha 410000, Hunan, Peoples R China.;[Liu, Yu; Shi, Jian-Ping; Shi, Zhi-Qiang] Inner Mongolia Med Univ, Hohhot 010000, Inner Mongolia, Peoples R China.;[Xiong, Wu] Hunan Univ Chinese Med, Affiliated Hosp 1, Dept Burn & Plast Surg, Changsha 410007, Hunan, Peoples R China.
通讯机构：
[Zhou, Jian-Da] D;Department of Plastic Surgery, The Third Xiangya Hospital, Central South University, Changsha, P.R. China
摘要：
The wound-healing process is a natural response to burn injury. Resveratrol (RES) may have potential as a therapy for wound healing, but how and whether RES regulates skin repair remains poorly understood. Human epidermal keratinocyte (HaCaT) cells were treated with lipopolysaccharide (LPS), and a mouse skin wound-healing model was established. Cell viability and apoptosis were analyzed by 3-(4,5-dimethyl-2-thiazolyl)−2,5-diphenyl-2-H-tetrazolium bromide or flow cytometry. Cell proliferation was assessed by cell viability and colony-formation analyses. Cell migration was tested by wound-healing analysis. The microRNA-212 (miR-212) and caspase-8 (CASP8) levels were determined by quantitative reverse transcription polymerase chain reaction and western blotting. The correlation between miR-212 and CASP8 was analyzed by dual-luciferase reporter analysis. Skin wound healing in mice was assessed by measuring the wound area and gap after hematoxylin–eosin (HE) staining. RES reduced the LPS-induced reduction in viability and apoptosis in HaCaT cells. miR-212 expression was reduced by LPS and increased by exposure to RES. RES promoted cell proliferation and migration after LPS treatment by increasing miR-212 levels. CASP8 was a target of miR-212. CASP8 silencing promoted cell proliferation and migration, which was reversed by miR-212 knockdown in LPS-treated HaCaT cells. RES promoted skin wound healing in mice, which was reduced by miR-212 knockdown. Thus, RES facilitates cell proliferation and migration in LPS-treated HaCaT cells and promotes skin wound-healing in a mouse model by regulating the miR-212/CASP8 axis. The authors aimed to provide new insights into the pathogenesis and treatment of cutaneous burns. They show that the plant polyphenol resveratrol contributes to cell proliferation and migration in lipopolysaccharide-stimulated human epidermal keratinocyte cells. Resveratrol promotes wound healing in a mouse skin wound model via regulation of the miR-212/CASP8 axis.
作者机构：
[肖美凤] College of Pharmacy, Hunan University of Chinese Medicine Changsha 410208, China Hunan Provincial Key Laboratory of Drugability and Preparation Modification of Traditional Chinese Medicine Changsha 410208, China;[段晓鹏] College of Pharmacy, Hunan University of Chinese Medicine Changsha 410208, China Supramolecular Mechanism and Mathematic-Physics Chracterization for Chinese Materia Medica, Hunan University of Chinese Medicine Changsha 410208, China;[邓凯文] The First Affinity Hospital, Hunan University of Chinese Medicine Changsha 410007, China;[刘文龙; 贺福元; 杨岩涛] College of Pharmacy, Hunan University of Chinese Medicine Changsha 410208, China Hunan Provincial Key Laboratory of Drugability and Preparation Modification of Traditional Chinese Medicine Changsha 410208, China Supramolecular Mechanism and Mathematic-Physics Chracterization for Chinese Materia Medica, Hunan University of Chinese Medicine Changsha 410208, China
通讯机构：
The First Affinity Hospital, Hunan University of Chinese Medicine, Changsha, China
摘要：
Long noncoding RNA-steroid receptor RNA activator (LncRNA-SRA) is transcribed from a class of noncoding genes, and plays a critical role in regulating cell proliferation. However, the effect of lncRNA-SRA remains unclear in vascular proliferative diseases. In the present study, we overexpressed lncRNA-SRA in vitro, then investigated the biological consequences. A vascular damage mice model was constructed by performing femoral artery wire injury. LncRNA-SRA was overexpressed in the injured arteries, and significantly promoted the expression of ki67, thereby caused an overall increase in neointima formation. LncRNA-SRA overexpression led to the proliferation and migration of vascular smooth muscle cells (VSMCs). By stimulating the phosphorylation of MEK, ERK and CREB (cyclic nucleotide responsive element binding protein), lncRNA-SRA promoted VSMC proliferation. Meanwhile, these effects were blocked by the MEK inhibitor U0126. Therefore, lncRNA-SRA promoted VSMC proliferation by activating the MEK-ERK-CREB pathway. LncRNA-SRA could be a promising therapeutic target in vascular diseases characterized by neointimal hyperplasia.
作者机构：
[朱鼎铭; 王超; 谭成富; 刘薇薇; 杜琳; 唐雅妮; 郭礼娜; 陈美琳; 李姣兰] College of Acupuncture-moxibustion and Massage, Hunan University of Chinese Medicine, Changsha 410007, China;[章薇] Department of Acupuncture and Moxibustion of the First Affiliated Hospital, Hunan University of Chinese Medicine, Changsha 410007
作者机构：
[Gu, Qianbiao] Department of Radiology, Third Xiangya Hospital, Central South University, Changsha 410013;[Liu, Peng; Gu, Qianbiao] Department of Radiology, People's Hospital of Hunan Province, First Affiiated Hospital, Hunan Normal University, Changsha 410002, China;[Feng, Zhichao; Ma, Mengtian; Rong, Pengfei; Yan, Haixiong] Department of Radiology, Third Xiangya Hospital, Central South University, Changsha 410013, China;[Hu, Xiaoli] First Hospital of Hunan University of Chinese Medicine, Changsha 410007, China;[Mustafa Jumbe, Mwajuma] Department of Radiology, Muhimbili National Hospital, Dar es Salaam 65000, Tanzania
通讯机构：
Department of Radiology, Third Xiangya Hospital, Central South University, Changsha, China
期刊：
Mediators of Inflammation,2019年2019:6453296 ISSN：0962-9351
通讯作者：
Xing, Wei;Xiao, Xian-Zhong
作者机构：
[Peng, Yue; Xing, Wei; Yang, Ming-Shi; Wang, Qian-Lu; Gao, Min] Cent South Univ, Dept Intens Care Med, Xiangya Hosp 3, Changsha 410013, Hunan, Peoples R China.;[Yang, Lei] Hunan Univ Chinese Med, Hosp 1, Dept Pharm, Changsha 410003, Hunan, Peoples R China.;[Xiao, Xian-Zhong] Cent South Univ, Dept Pathophysiol, Xiangya Sch Med, Changsha 410078, Hunan, Peoples R China.
通讯机构：
[Xing, Wei; Xiao, Xian-Zhong] C;Cent South Univ, Dept Intens Care Med, Xiangya Hosp 3, Changsha 410013, Hunan, Peoples R China.;Cent South Univ, Dept Pathophysiol, Xiangya Sch Med, Changsha 410078, Hunan, Peoples R China.
摘要：
Objectives: To investigate the protective effect of ginsenoside Rg1 on relieving sepsis-induced lung inflammation and injury in vivo and in vitro. Methods: Cultured human pulmonary epithelial cell line A549 was challenged with LPS to induce cell injury, and CLP mouse model was generated to mimic clinical condition of systemic sepsis. Rg1 was applied to cells or animals at indicated dosage. Apoptosis of cultured cells was quantified by flow cytometry, along with ELISA for inflammatory cytokines in supernatant. For septic mice, lung tissue pathology was examined, plus ELISA assay for serum cytokines. Western blotting was used to examine the activation of inflammatory pathways and ER stress marker proteins in both cells and mouse lung tissues. Reactive oxygen species (ROS) level was quantified by DCFDA kit. Results: Ginsenoside Rg1 treatment remarkably suppressed apoptosis rate of LPS-induced A549 cells, relieved mouse lung tissue damage, and elevated survival rate. Rg1 treatment also rescued cells from LPS-induced intracellular ROS. In both A549 cells and mouse lung tissues, further study showed that Rg1 perfusion significantly suppressed the secretion of inflammatory cytokines including tumor necrosis factor- (TNF-) alpha and interleukin- (IL-) 6 and relieved cells from ER stress as supported by decreased expression of marker proteins via upregulating sirtuin 1 (SIRT1). Conclusion: Our results showed that ginsenoside Rg1 treatment effectively relieved sepsis-induced lung injury in vitro and in vivo, mainly via upregulating SIRT1 to relieve ER stress and inflammation. These findings provide new insights for unrevealing potential candidate for severe sepsis accompanied with lung injury.
摘要：
BACKGROUND: Impaired wound healing in diabetes foot ulcers (DFUs) brings a great burden to diabetic patients. Pro-angiogenesis through elevating nitric oxide (NO) is beneficial to the wound healing process. Ginsenoside Rg1, the main active in Notoginseng, is reported to regulate the angiogenesis in endothelial cells through modulating miR-23a. However, the effect of Rg1 in diabetes remains elusive. METHODS: High fat diet combined with streptozotocin-induced diabetic rats were treated with Rg1. Then incision area and tissue NO level were measured to evaluate the wound closure efficacy of Rg1. Then high glucose cultured HUVECs were employed to mimic diabetic environment in vitro. Overexpression and knockdown plasmids of miR-23a or IRF-1 were constructed and transfected in HUVECs. qPCR and western blot were used to determine the mRNA and protein level, respectively. Dual-luciferase reporter assay was utilized to determine the interaction of IRF-1/miR-23a. RESULTS: Rg1 accelerated the wound closure speed in diabetic rats and increased NO level through elevating iNOS expression. Knockdown of iNOS reversed Rg1-induced VEGF expression, cell proliferation, anti-apoptotic efficacy and cell migration ability in high glucose cultured HUVECs. Further investigation revealed that Rg1 mediated iNOS through miR-23a. miR-23a inhibited the expression of IRF-1, a protein which could directly bind to the iNOS mRNA 3'UTR. CONCLUSION: Rg1 promoted angiogenesis in diabetic wound healing process through NO signaling via miR-23a, providing a novel candidate for DFUs treatment.
期刊：
Digestive and Liver Disease,2019年51(3):425-433 ISSN：1590-8658
通讯作者：
Wang, Xianbo;Sun, Kewei;Li, Hai
作者机构：
[Gao, Fangyuan; Liu, Yao; Wang, Xianbo] Capital Med Univ, Beijing Ditan Hosp, Ctr Integrat Med, Beijing 100015, Peoples R China.;[Sun, Kewei; Zhang, Qianqian] Hunan Univ Chinese Med, Hosp 1, Dept Hepatol, Changsha 410007, Hunan, Peoples R China.;[Gong, Guozhong] Ctr South Univ, Xiangya Hosp 2, Dept Infect Dis, Changsha, Hunan, Peoples R China.;[Mao, Dewen] Guangxi Univ Chinese Med, Affiliated Hosp 1, Dept Hepatol, Nanning, Peoples R China.;[Gong, Zuojiong] Wuhan Univ, Renmin Hosp, Dept Infect Dis, Wuhan, Hubei, Peoples R China.
通讯机构：
[Wang, Xianbo] C;[Sun, Kewei] H;[Li, Hai] S;Capital Med Univ, Beijing Ditan Hosp, Ctr Integrat Med, Beijing 100015, Peoples R China.;Hunan Univ Chinese Med, Hosp 1, Dept Hepatol, Changsha 410007, Hunan, Peoples R China.
关键词：
Acute-on-chronic liver failure;Hepatitis B virus;Nomogram;Prognosis
摘要：
BACKGROUND: The current definitions and etiologies of acute-on-chronic liver failure (ACLF) are clearly very different between East and West. AIMS: This study aimed to develop an effective prognostic nomogram for acute-on-chronic hepatitis B liver failure (ACHBLF) as defined by the Asia Pacific Association for the Study of the Liver (APASL). METHODS: The nomogram was based on a retrospective study of 573 patients with ACHBLF, defined according to the APASL, at the Beijing Ditan Hospital. The results were validated using a bootstrapped approach to correct for bias in two external cohorts, including an APASL ACHBLF cohort (10 hospitals, N=329) and an EASL-CLIF ACHBLF cohort (Renji Hospital, N=300). RESULTS: Multivariate analysis of the derivation cohort for survival analysis helped identify the independent factors as age, total bilirubin, albumin, international normalized ratio, and hepatic encephalopathy, which were included in the nomogram. The predictive value of nomogram was the strongest compared with CLIF-C ACLF, MELD and MELD-Na and similar to COSSH-ACLF in both the derivation and prospective validation cohorts with APASL ACHBLF, but the CLIF-C ACLF was better in the EASL-CLIF ACHBLF cohort. CONCLUSIONS: The proposed nomogram could accurately estimate individualized risk for the short-term mortality of patients with ACHBLF as defined by APASL.
作者：
Zhang, P.;Du, H. B.;Tong, G. D.;Li, X. K.;Sun, X. H.;...
期刊：
Journal of Viral Hepatitis,2018年25(9):1017-1025 ISSN：1352-0504
通讯作者：
Zhou, D. Q.;Ye, Y. A.;Gao, Y. Q.
作者机构：
[Zhang, P.; Du, H. B.; Ye, Y. A.; Li, X. K.; Jiang, F.] Beijing Univ Chinese Med, Affiliated Dongzhimen Hosp, Dept Gastroenterol & Hepatol, Beijing, Peoples R China.;[Zhang, P.; Du, H. B.; Ye, Y. A.; Yang, X. Z.; Li, X. K.; Jiang, F.] Beijing Univ Chinese Med, Affiliated Dongzhimen Hosp, Inst Liver Dis, Beijing, Peoples R China.;[Xing, Y. F.; Zheng, Y. J.; Zhou, D. Q.; Tong, G. D.] Shenzhen Hosp Tradit Chinese Med, Dept Hepatol, Shenzhen, Guangdong, Peoples R China.;[Sun, X. H.; Gao, Y. Q.; Zhou, Z. H.; Zhao, G.] Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Dept Hepatol, Shanghai, Peoples R China.;[Chi, X. L.; Jiang, J. M.; Tian, G. J.] Guangdong Hosp Tradit Chinese Med, Dept Hepatol, Guangzhou, Guangdong, Peoples R China.
通讯机构：
[Zhou, D. Q.; Gao, Y. Q.] S;[Ye, Y. A.] B;Shenzhen Hosp Tradit Chinese Med, Dept Hepatol, Shenzhen, Guangdong, Peoples R China.;Beijing Univ Chinese Med, Affiliated Dongzhimen Hosp, Inst Liver Dis, Dept Gastroenterol & Hepatol, Beijing, Peoples R China.;Shuguang Hosp, Dept Hepatol, Shanghai, Peoples R China.
关键词：
affecting factor;HBsAg;HBV infection;multicentre trial;natural history
